Corticosterone Regulates the Expression of Neuropeptide Y and Reelin in MLO-Y4 Cells

Ma, Yuanyuan; Wu, Xiangnan; Li, Xianxian; Fu, Jing; Shen, Jiefei; Li, Xiaoyü; Wang, Hang

doi:10.1007/s10059-012-0053-y

Cited by 11 publications

(8 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As previously shown (34, 35, 50), and confirmed in the present study, osteoblasts and osteocytes synthesize NPY in vivo and in cell cultures of primary osteoblasts and osteo‐blast and osteocyte cell lines. Indeed, the expression of NPY is a well‐known marker of osteocyte differentiation (34, 51, 52).…”

Section: Discussionsupporting

confidence: 92%

p38α function in osteoblasts influences adipose tissue homeostasis

Rodríguez-Carballo

Gámez²,

Méndez-Lucas³

et al. 2014

FASEB j.

View full text Add to dashboard Cite

The skeleton acts as an endocrine organ that regulates energy metabolism and calcium and phosphorous homeostasis through the secretion of osteocalcin (Oc) and fibroblast growth factor 23 (FGF23). However, evidence suggests that osteoblasts secrete additional unknown factors that contribute to the endocrine function of bone. To search for these additional factors, we generated mice with a conditional osteoblast-specific deletion of p38a MAPK known to display profound defects in bone homeostasis. Herein, we show that impaired osteoblast function is associated with a strong decrease in body weight and adiposity (P < 0.01). The differences in adiposity were not associated with diminished caloric intake, but rather reflected 20% increased energy expenditure and the upregulation of uncoupling protein-1 (Ucp1) in white adipose tissue (WAT) and brown adipose tissue (BAT) (P < 0.05). These alterations in lipid metabolism and energy expenditure were correlated with a decrease in the blood levels of neuropeptide Y (NPY) (40% lower) rather than changes in the serum levels of insulin, Oc, or FGF23. Among all Npyexpressing tissues, only bone and primary osteoblasts showed a decline in Npy expression (P < 0.01). Moreover, the intraperitoneal administration of recombinant NPY partially restored the WAT weight and adipocyte size of p38a-deficient mice (P < 0.05). Altogether, these results further suggest that, in addition to Oc, other bone-derived signals affect WAT and energy expenditure contributing to the regulation of energy metabolism.-Rodríguez-

show abstract

Section: Discussionsupporting

confidence: 92%

p38α function in osteoblasts influences adipose tissue homeostasis

Rodríguez-Carballo

Gámez²,

Méndez-Lucas³

et al. 2014

FASEB j.

View full text Add to dashboard Cite

show abstract

“…Osteocyte-like MLOY4 cells were cultured as previously described (Kato et al, 1997;Ma et al, 2012). Mouse primary calvarial cells were prepared from the calvaria of neonatal mice as previously described (Park et al, 2007).…”

Section: Cell Culturementioning

confidence: 99%

Pax6 Expressed in Osteocytes Inhibits Canonical Wnt Signaling

Jami

Gadi

Lee

et al. 2013

Molecules and Cells

View full text Add to dashboard Cite

The transcription factor Pax6, which belongs to the paired box-containing gene family, regulates developmental processes, especially in the eyes, central nervous tissues and craniofacial structures. However, the role of Pax6 in bone has never been studied exclusively. Here we report that Pax6 is expressed at both the mRNA and protein level in the calvaria and long bones of adult mice as well as osteocyte-like MLOY4 cells and suppresses the canonical Wnt signaling pathway. Moreover, the expression levels of Pax6 were much higher in the calvaria than the long bones, and Pax6 was also expressed at E16 to E18 in both the calvaria and long bones. Knockdown of Pax6 in MLOY4 cells did not affect cell proliferation or survival; however, the expression of Sost, an osteocyte marker gene, was significantly decreased. In addition, the overexpression of Pax6 suppressed the canonical Wnt signaling pathway by enhancing the expression of Sost. Furthermore, we also demonstrated that Pax6 binds to the Sost promoter and that stimulation of Sost transcription by Pax6 was dependent on a specific Pax6-binding sequence within the promoter. In conclusion, the results of the present study suggest that Pax6 is expressed in bone and may play an important role in osteocyte differentiation by controlling canonical Wnt signaling.

show abstract

“…Reelin protein levels in the brain could be modified by several factors such as hormones [20][21][22][23][24], oxidative stress [25], perinatal stress [26], and exercise [27]. Some of these conditions (e.g., hormone misbalance and oxidative stress) are common features in diseases such as schizophrenia [28,29] and autism [30], as well as neurodegenerative diseases such as Alzheimer's disease [31,32] and prionopathies [33].…”

Section: Introductionmentioning

confidence: 99%

Reelin Expression in Creutzfeldt-Jakob Disease and Experimental Models of Transmissible Spongiform Encephalopathies

et al. 2016

View full text Add to dashboard Cite

Reelin is an extracellular glycoprotein involved in key cellular processes in developing and adult nervous system, including regulation of neuronal migration, synapse formation, and plasticity. Most of these roles are mediated by the intracellular phosphorylation of disabled-1 (Dab1), an intracellular adaptor molecule, in turn mediated by binding Reelin to its receptors. Altered expression and glycosylation patterns of Reelin in cerebrospinal and cortical extracts have been reported in Alzheimer's disease. However, putative changes in Reelin are not described in natural prionopathies or experimental models of prion infection or toxicity. With this is mind, in the present study, we determined that Reelin protein and mRNA levels increased in CJD human samples and in mouse models of human prion disease in contrast to murine models of prion infection. However, changes in Reelin expression appeared only at late terminal stages of the disease, which prevent their use as an efficient diagnostic biomarker. In addition, increased Reelin in CJD and in in vitro models does not correlate with Dab1 phosphorylation, indicating failure in its intracellular signaling. Overall, these findings widen our understanding of the putative changes of Reelin in neurodegeneration.

show abstract

Corticosterone Regulates the Expression of Neuropeptide Y and Reelin in MLO-Y4 Cells

Cited by 11 publications

References 44 publications

p38α function in osteoblasts influences adipose tissue homeostasis

p38α function in osteoblasts influences adipose tissue homeostasis

Pax6 Expressed in Osteocytes Inhibits Canonical Wnt Signaling

Reelin Expression in Creutzfeldt-Jakob Disease and Experimental Models of Transmissible Spongiform Encephalopathies

Contact Info

Product

Resources

About